scholarly journals Electrical Detection of Innate Immune Cells

Sensors ◽  
2021 ◽  
Vol 21 (17) ◽  
pp. 5886
Author(s):  
Mahmoud Al Ahmad ◽  
Rasha A. Nasser ◽  
Lillian J. A. Olule ◽  
Bassam R. Ali
Keyword(s):  
Image Processing ◽  
Cell Size ◽  
Inflammatory Diseases ◽  
Rapid Development ◽  
Electrical Characterization ◽  
Cell Types ◽  
Innate Immune ◽  
Electrical Measurements ◽  
Reliable Marker

Accurately classifying the innate immune players is essential to comprehensively and quantitatively evaluate the interactions between the innate and the adaptive immune systems. In addition, accurate classification enables the development of models to predict behavior and to improve prospects for therapeutic manipulation of inflammatory diseases and cancer. Rapid development in technologies that provide an accurate definition of the type of cell in action, allows the field of innate immunity to the lead in therapy developments. This article presents a novel immunophenotyping technique using electrical characterization to differentiate between the two most important cell types of the innate immune system: dendritic cells (DCs) and macrophages (MACs). The electrical characterization is based on capacitance measurements, which is a reliable marker for cell surface area and hence cell size. We differentiated THP-1 cells into DCs and MACs in vitro and conducted electrical measurements on the three cell types. The results showed average capacitance readings of 0.83 µF, 0.93 µF, and 1.01 µF for THP-1, DCs, and MACs, respectively. This corresponds to increasing cell size since capacitance is directly proportional to area. The results were verified with image processing. Image processing was used for verification because unlike conventional techniques, especially flow cytometry, it avoids cross referencing and by-passes the limitation of a lack of specificity of markers used to detect the different cell types.

scholarly journals Heme Oxygenase-1 Deficiency and Oxidative Stress: A Review of 9 Independent Human Cases and Animal Models

2021 ◽  
Vol 22 (4) ◽  
pp. 1514 ◽  
Author(s):  
Akihiro Yachie
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Heme Oxygenase ◽  
Inflammatory Diseases ◽  
Cell Types ◽  
Pharmacological Intervention ◽  
Heme Oxygenase 1 ◽  
Inflammatory Reactions

Since Yachie et al. reported the first description of human heme oxygenase (HO)-1 deficiency more than 20 years ago, few additional human cases have been reported in the literature. A detailed analysis of the first human case of HO-1 deficiency revealed that HO-1 is involved in the protection of multiple tissues and organs from oxidative stress and excessive inflammatory reactions, through the release of multiple molecules with anti-oxidative stress and anti-inflammatory functions. HO-1 production is induced in vivo within selected cell types, including renal tubular epithelium, hepatic Kupffer cells, vascular endothelium, and monocytes/macrophages, suggesting that HO-1 plays critical roles in these cells. In vivo and in vitro studies have indicated that impaired HO-1 production results in progressive monocyte dysfunction, unregulated macrophage activation and endothelial cell dysfunction, leading to catastrophic systemic inflammatory response syndrome. Data from reported human cases of HO-1 deficiency and numerous studies using animal models suggest that HO-1 plays critical roles in various clinical settings involving excessive oxidative stress and inflammation. In this regard, therapy to induce HO-1 production by pharmacological intervention represents a promising novel strategy to control inflammatory diseases.

scholarly journals Could Chlamydia Pneumoniae Be Considered an Infectious Risk Factor for Inflammatory Diseases Such as Atherosclerosis ?

2005 ◽  
Vol 3 (3) ◽  
pp. 109-112
Author(s):  
R. Sessa ◽  
M. Di Pietro ◽  
G. Schiavoni ◽  
I. Santino ◽  
M. Del Piano
Keyword(s):  
Risk Factor ◽  
Chlamydia Pneumoniae ◽  
Direct Detection ◽  
Inflammatory Diseases ◽  
Cell Types ◽  
Chronic Inflammatory Disease ◽  
Upper Respiratory Tract ◽  
Infectious Risk ◽  
Tract Infections

Chlamydia pneumoniae, a Gram-negative intracellular obligate bacteria, is recognised as a common cause of upper respiratory tract infections, and accounts for ∼10% of community-acquired pneumonia. In recent years, chronic and persistent infection with C. pneumoniae has been implicated in the pathogenesis of atherosclerosis. Atherosclerosis is regarded as a chronic inflammatory disease that results from complex interactions between a variety of cell types such as endothelial cells, vascular smooth muscle cells, monocytes/macrophages and inflammatory mediators. Involvement of C. pneumoniae in the pathogenesis of atherosclerosis has been supported by findings from seroepidemiologic studies, direct detection of chlamydial DNA, experimental animal and in vitro studies, and antibiotic intervention trials. The spectrum of cell biological, animal, and human clinical data suggests that C. pneumoniae may be considered an infectious risk factor for atherosclerosis but further studies are needed to clarify the etiopathogenetic role of C. pneumoniae in atherosclerotic vessel walls.

scholarly journals Gold Nanoparticles Modulate BCG-Induced Innate Immune Memory in Human Monocytes by Shifting the Memory Response towards Tolerance

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 284 ◽  
Author(s):  
Benjamin J. Swartzwelter ◽  
Francesco Barbero ◽  
Alessandro Verde ◽  
Maria Mangini ◽  
Marinella Pirozzi ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Secondary Response ◽  
Immune Memory ◽  
Inflammatory Factor ◽  
Memory Response ◽  
Lps Challenge ◽  
Anti Inflammatory

Innate immune memory is characterized by a modulation in the magnitude with which innate immune cells such as monocytes and macrophages respond to potential dangers, subsequent to previous exposure to the same or unrelated agents. In this study, we have examined the capacity of gold nanoparticles (AuNP), which are already in use for therapeutic and diagnostic purposes, to modulate the innate memory induced by bacterial agents. The induction of innate memory was achieved in vitro by exposing human primary monocytes to bacterial agents (lipopolysaccharide -LPS-, or live Bacille Calmette-Guérin -BCG) in the absence or presence of AuNP. After the primary activation, cells were allowed to return to a resting condition, and eventually re-challenged with LPS. The induction of memory was assessed by comparing the response to the LPS challenge of unprimed cells with that of cells primed with bacterial agents and AuNP. The response to LPS was measured as the production of inflammatory (TNFα, IL-6) and anti-inflammatory cytokines (IL-10, IL-1Ra). While ineffective in directly inducing innate memory per se, and unable to influence LPS-induced tolerance memory, AuNP significantly affected the memory response of BCG-primed cells, by inhibiting the secondary response in terms of both inflammatory and anti-inflammatory factor production. The reprogramming of BCG-induced memory towards a tolerance type of reactivity may open promising perspectives for the use of AuNP in immunomodulatory approaches to autoimmune and chronic inflammatory diseases.

Functional characterization of alpha- and beta-intercalated cell types in rabbit cortical collecting duct

1991 ◽  
Vol 261 (3) ◽  
pp. F377-F385 ◽  
Author(s):  
H. Furuya ◽  
M. D. Breyer ◽  
H. R. Jacobson
Keyword(s):  
Collecting Duct ◽  
Basolateral Membrane ◽  
Functional Characterization ◽  
Cell Types ◽  
Disulfonic Acid ◽  
Cortical Collecting Duct ◽  
Electrical Measurements ◽  
Collecting Ducts

Single-cell electrical measurements and spectrophotometric determinations of intracellular pH were used to determine unique features of alpha- and beta-intercalated cells (alpha-IC, beta-IC) in in vitro perfused rabbit cortical collecting ducts (CCD). pHi rose in alpha-IC and fell in beta-IC after bath Cl- removal. Luminal Cl- removal did not change pHi of alpha-IC, but pHi of beta-IC rose by 0.36 +/- 0.01 pH units. Cl- concentration-dependent recovery of beta-IC pHi revealed a Cl- Km of 18.7 mM for the luminal Cl(-) -HCO3- exchanger. Measurements of basolateral membrane voltage (Vbl) also showed two IC cell types. Removal of luminal Cl- did not change Vbl in alpha-IC, whereas Vbl hyperpolarized by a mean of 73.2 +/- 3.5 mV in beta-IC. Reducing bath Cl- depolarized both alpha- and beta-IC Vbl. In alpha-IC a large repolarization of 39.8 +/- 5.2 mV followed acute depolarization after bath Cl- removal. Reducing bath HCO3- (constant CO2) had little effect on beta-IC Vbl, whereas alpha-IC Vbl depolarized by 5.2 +/- 0.7 mV. Reducing luminal HCO3- in the absence of luminal Cl- produced a 17.6 +/- 1.8 mV depolarization in beta-IC. This change was independent of luminal Na+ and was not blocked by luminal 10(-4) M 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). In beta-IC, Vbl was not altered by either bath or lumen DIDS in the presence of luminal Cl-. However, when luminal Cl- was removed, luminal DIDS reversibly depolarized Vbl by 9.6 +/- 2.9 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Identification of an ASC oligomerization inhibitor for the treatment of inflammatory diseases

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Paula M. Soriano-Teruel ◽  
Guillermo García‑Laínez ◽  
María Marco-Salvador ◽  
Julián Pardo ◽  
Maykel Arias ◽  
...  
Keyword(s):  
Innate Immune System ◽  
Inflammatory Cell ◽  
Inflammatory Diseases ◽  
Primary Cultures ◽  
Innate Immune ◽  
Cytokine Release ◽  
Multifactorial Diseases ◽  
Molecule Inhibitor

AbstractThe ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD)) protein is an scaffold component of different inflammasomes, intracellular multiprotein platforms of the innate immune system that are activated in response to pathogens or intracellular damage. The formation of ASC specks, initiated by different inflammasome receptors, promotes the recruitment and activation of procaspase-1, thereby triggering pyroptotic inflammatory cell death and pro-inflammatory cytokine release. Here we describe MM01 as the first-in-class small-molecule inhibitor of ASC that interferes with ASC speck formation. MM01 inhibition of ASC oligomerization prevents activation of procaspase-1 in vitro and inhibits the activation of different ASC-dependent inflammasomes in cell lines and primary cultures. Furthermore, MM01 inhibits inflammation in vivo in a mouse model of inflammasome-induced peritonitis. Overall, we highlight MM01 as a novel broad-spectrum inflammasome inhibitor for the potential treatment of multifactorial diseases involving the dysregulation of multiple inflammasomes.

scholarly journals The ORF4b-encoded accessory proteins of Middle East respiratory syndrome coronavirus and two related bat coronaviruses localize to the nucleus and inhibit innate immune signalling

2014 ◽  
Vol 95 (4) ◽  
pp. 874-882 ◽  
Author(s):  
Krystal L. Matthews ◽  
Christopher M. Coleman ◽  
Yvonne van der Meer ◽  
Eric J. Snijder ◽  
Matthew B. Frieman
Keyword(s):  
Middle East ◽  
Severe Pneumonia ◽  
Cell Types ◽  
Innate Immune ◽  
Middle East Respiratory Syndrome ◽  
Signalling Pathways ◽  
Type I ◽  
Accessory Proteins ◽  
Type I Ifn

The recently emerged Middle East respiratory syndrome coronavirus (MERS-CoV), a betacoronavirus, is associated with severe pneumonia and renal failure. The environmental origin of MERS-CoV is as yet unknown; however, its genome sequence is closely related to those of two bat coronaviruses, named BtCoV-HKU4 and BtCoV-HKU5, which were derived from Chinese bat samples. A hallmark of highly pathogenic respiratory viruses is their ability to evade the innate immune response of the host. CoV accessory proteins, for example those from severe acute respiratory syndrome CoV (SARS-CoV), have been shown to block innate antiviral signalling pathways. MERS-CoV, similar to SARS-CoV, has been shown to inhibit type I IFN induction in a variety of cell types in vitro. We therefore hypothesized that MERS-CoV and the phylogenetically related BtCoV-HKU4 and BtCoV-HKU5 may encode proteins with similar capabilities. In this study, we have demonstrated that the ORF4b-encoded accessory protein (p4b) of MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 may indeed facilitate innate immune evasion by inhibiting the type I IFN and NF-κB signalling pathways. We also analysed the subcellular localization of p4b from MERS-CoV, BtCoV-HKU4 and BtCoV-HKU5 and demonstrated that all are localized to the nucleus.

scholarly journals Mesenchymal Stromal Cells Support Endometriotic Stromal CellsIn Vitro

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Fawaz Abomaray ◽  
Sebastian Gidlöf ◽  
Bartosz Bezubik ◽  
Mikael Engman ◽  
Cecilia Götherström
Keyword(s):  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Inflammatory Diseases ◽  
Umbilical Vein ◽  
Cell Types ◽  
Tube Formation ◽  
Migration And Invasion ◽  
Endometrial Cells ◽  
Umbilical Vein Endothelial Cells

Endometriosis is an inflammatory disease marked by ectopic growth of endometrial cells. Mesenchymal stromal cells (MSC) have immunosuppressive properties that have been suggested as a treatment for inflammatory diseases. Therefore, the aim herein was to examine effects of allogeneic MSC on endometriosis-derived cellsin vitroas a potential therapy for endometriosis. MSC from allogeneic adipose tissue (Ad-MSC) and stromal cells from endometrium (ESCendo) and endometriotic ovarian cysts (ESCcyst) from women with endometriosis were isolated. The effects of Ad-MSC on ESCendoand ESCcystwere investigated usingin vitroproliferation, apoptosis, adhesion, tube formation, migration, and invasion assays. Ad-MSC significantly increased proliferation of ESC compared to untreated controls. Moreover, Ad-MSC significantly decreased apoptosis and increased survival of ESC. Ad-MSC significantly increased adhesion of ESCendoand not ESCcyston fibronectin. Conditioned medium from cocultures of Ad-MSC and ESC significantly increased tube formation of human umbilical vein endothelial cells on matrigel. Ad-MSC may significantly increase migration of ESCcystand did not increase invasion of both cell types. The data suggest that allogeneic Ad-MSC should not be considered as a potential therapy for endometriosis, because they may support the pathology by maintaining and increasing growth of ectopic endometrial tissue.

scholarly journals Cysteinyl Leukotriene Receptor-1 Antagonists as Modulators of Innate Immune Cell Function

2014 ◽  
Vol 2014 ◽  
pp. 1-16 ◽  
Author(s):  
A. J. Theron ◽  
H. C. Steel ◽  
G. R. Tintinger ◽  
C. M. Gravett ◽  
R. Anderson ◽  
...  
Keyword(s):  
Cell Function ◽  
Immune Cell ◽  
Cell Types ◽  
Innate Immune ◽  
Human Neutrophils ◽  
Cysteinyl Leukotriene ◽  
Anti Inflammatory ◽  
Cysteinyl Leukotriene Receptor ◽  
Underlying Mechanisms

Cysteinyl leukotrienes (cysLTs) are produced predominantly by cells of the innate immune system, especially basophils, eosinophils, mast cells, and monocytes/macrophages. Notwithstanding potent bronchoconstrictor activity, cysLTs are also proinflammatory consequent to their autocrine and paracrine interactions with G-protein-coupled receptors expressed not only on the aforementioned cell types, but also on Th2 lymphocytes, as well as structural cells, and to a lesser extent neutrophils and CD8+cells. Recognition of the involvement of cysLTs in the immunopathogenesis of various types of acute and chronic inflammatory disorders, especially bronchial asthma, prompted the development of selective cysLT receptor-1 (cysLTR1) antagonists, specifically montelukast, pranlukast, and zafirlukast. More recently these agents have also been reported to possess secondary anti-inflammatory activities, distinct from cysLTR1 antagonism, which appear to be particularly effective in targeting neutrophils and monocytes/macrophages. Underlying mechanisms include interference with cyclic nucleotide phosphodiesterases, 5′-lipoxygenase, and the proinflammatory transcription factor, nuclear factor kappa B. These and other secondary anti-inflammatory mechanisms of the commonly used cysLTR1 antagonists are the major focus of the current review, which also includes a comparison of the anti-inflammatory effects of montelukast, pranlukast, and zafirlukast on human neutrophilsin vitro, as well as an overview of both the current clinical applications of these agents and potential future applications based on preclinical and early clinical studies.

CC chemokine receptor 5 gene promoter activation by the cyclic AMP response element binding transcription factor

Blood ◽  
2008 ◽  
Vol 112 (5) ◽  
pp. 1610-1619 ◽  
Author(s):  
Hedwich F. Kuipers ◽  
Paula J. Biesta ◽  
Lisette J. Montagne ◽  
Elise S. van Haastert ◽  
Paul van der Valk ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Stress Responses ◽  
Inflammatory Diseases ◽  
Transplant Rejection ◽  
Cell Types ◽  
In Vitro Assays ◽  
Specific Expression ◽  
Mhc Molecules ◽  
Creb Pathway

Abstract The chemokine receptor CCR5 is implicated in the pathogenesis of various inflammatory diseases, such as multiple sclerosis (MS), atherosclerosis, transplant rejection, and autoimmunity. In previous studies, we have shown that MS lesions are characterized by enhanced expression of transcription factors associated with stress responses, ie, IRF-1, NF-κB, and CREB-1, which modulate expression of both classes of major histocompatibility complex (MHC) molecules. The expression of MHC-I and MHC-II molecules greatly overlaps with the expression of CCR5 in MS lesions. Therefore, we investigated whether these factors are also involved in the transcriptional regulation of CCR5. Using in vitro assays, we determined that neither IRF-1 nor NF-κB is involved in the activation of the CCR5 promoter. This is corroborated by the finding that these factors are not involved in the induction of endogenous CCR5 transcription in various cell types. In contrast, we show that CCR5 expression is regulated by the cAMP/CREB pathway and that interference in this pathway affects endogenous CCR5 transcription. From this, we conclude that the cAMP/CREB pathway is involved in the regulation of CCR5 transcription and that, given the ubiquitous nature of CREB-1 protein expression, additional regulatory mechanisms must contribute to cell type-specific expression of CCR5.

Physical and Electrical Performance Comparison of Identical 28 nm Qualcomm Telecommunication Die Produced by Samsung and TSMC

2013 ◽  
Author(s):  
Anton Riley ◽  
Sean Zumwalt ◽  
Sinjin Dixon-Warren ◽  
Gary Tomkins
Keyword(s):  
Rapid Development ◽  
Electrical Characterization ◽  
Performance Comparison ◽  
Advanced Technology ◽  
Electrical Performance ◽  
Reference Source ◽  
Electrical Measurements ◽  
Speed To Market ◽  
4G Lte ◽  
28 Nm

Abstract In today’s competitive semiconductor environment, product performance and market timing has never been more valuable. Design IP, speed to market, and taking advantage of the most advanced technology are three ways fabless companies can maintain an advantage over the competition. Foundries target these demands by offering superior support, competitive technology, and rapid development cycles. Using the advanced tool suites of SEM, FIB, TEM, and Atomic Force NanoProbing (AFP) the failure analysis community now has the ability to investigate and compare foundry performance on the device level. The 28 nm LP Qualcomm “SHELBY” die is dual-sourced from both Samsung and TSMC, and is the primary die in the MDM9215 4G/LTE modem used in several smartphones. This represents a unique case of leading technology, available to the public, to qualify for electrical performance on the device level using the AFP and the corresponding physical differences using SEM and TEM. These advanced FA techniques were employed and were able to identify manufacturing differences between foundries. They were then used to relate the physical variations with the electrical device performance. The HG11-N3877 fabricated by TSMC and the HG11-N9204 fabricated by Samsung were the subjects of this comparison (see Error! Reference source not found.). The investigation located spatial and geometric variations of the SRAM devices using cross sectioning and TEM imaging. This was followed by Electrical Characterization of multiple SRAM Cells using the AFP. The electrical measurements showed clear differences in device parameters. These differences highlight manufacturing process differences between the two companies that could directly relate to chip performance.

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